Effects of captopril on arterial and venous pressure, renal function, and humoral factors in severe chronic congestive heart failure.

The effects of captopril in several humoral factors were studied to elucidate the role of the renin-angiotensin (RA) system in arterial and venous pressures and renal function in patients with severe chronic congestive heart failure. A single oral dose of captopril in 20 subjects reduced mean arterial blood pressure from 77 to 67 mm Hg; this decrease correlated with baseline plasma renin activity (PRA). The increase in PRA and the decrease in plasma aldosterone levels after captopril were much greater in subjects with higher PRA. Plasma norepinephrine (NE) levels decreased, while those of epinephrine did not change. Peripheral venous pressure declined from 107 to 77 mm H2O; this decrease correlated with the change in NE levels. During 7-day captopril therapy, urine volume and sodium excretion increased (1145 to 1136 ml/day and 76 to 94 mEq/day) in 11 subjects in whom renal function was followed. Renal plasma flow (RPF) rose from 237 to 364 ml/min, while glomerular filtration rate did not change; the filtration fraction decreased from 32% to 23%. Simultaneous infusion of aprotinin in six of the subjects did not affect the captopril-induced increase in RPF, despite the suppression of plasma bradykinin levels. These results suggest that captopril reduces arterial blood pressure in patients with high PRA through inhibition of the RA system and dilates veins by attenuation of sympathetic nervous activity. Increased RPF and urinary sodium excretion induced by captopril might result from inhibition of the RA system; the kallikrein-kinin system or bradykinin-mediated prostaglandins do not appear to play a major role.